...PHILADELPHIA The AACR will present the 2011 AACR-Prevent Cancer Found...Dannenberg's work has provided the basis for the transformative discov...The AACR-Prevent Cancer Foundation Award for Excellence in Cancer Prev...Dannenberg's significant contributions include demonstrating that COX-...

PHILADELPHIA The AACR will present the 2011 AACR-Prevent Cancer Foundation Award for Excellence in Cancer Prevention Research to Andrew J. Dannenberg, M.D., at the 10th AACR International Conference on Frontiers in Cancer Prevention Research, held Oct. 22-25, 2011. Dannenberg is director of the Weill Cornell Cancer Center and director of cancer prevention at New York-Presbyterian/Weill Cornell Medical Center. He is also the Henry R. Erle, M.D.-Roberts Family Professor of Medicine at Weill Cornell Medical College.

Dannenberg's work has provided the basis for the transformative discovery linking obesity, inflammation and breast cancer. He is recognized for his work on the inflammation-cancer connection with an emphasis on prostaglandin biology. Dannenberg's research has been of major importance in explaining why levels of procarcinogenic prostaglandins are increased in inflamed tissues and tumors. He has also made major contributions to our understanding of why nonsteroidal anti-inflammatory drugs show chemopreventive activity.

The AACR-Prevent Cancer Foundation Award for Excellence in Cancer Prevention Research is given annually for seminal laboratory, translational, clinical, epidemiological or behavioral science contributions to the field of cancer prevention.

Dannenberg's significant contributions include demonstrating that COX-2 was overexpressed in a variety of premalignant lesions and cancers; elucidating the mechanisms by which oncogenes, tumor suppressor genes, carcinogens and tumor promoters regulate COX-2 gene expression; utilizing both pharmacological and genetic strategies to establish the importance of targeting prostaglandin synthesis as a bona fide prevention strategy; defining the signal transduction pathways by which dietary and synthetic chemopreventive agents suppress COX-2 transcription and prostaglandin synthesis; and determining the signaling mechanism by which COX-derived prostaglandin E2 induced aromatase, the rate-limiting enzyme responsible for estrogen synthesis. This latter work led to an observational study in which the use of aspirin was associated with a reduced risk for hormone receptor-positive breast cancer.

In his most recent work that provides new insights into the link between obesity, inflammation and breast cancer, Dannenberg conducted a preclinical study in which he used experimental models to demonstrate the presence of the obesityinflammationaromatase axis in the mammary gland. As a result, COX-2-derived PGE2 appeared to play an important role in inducing aromatase in the mammary glands of obese mice. Subsequently, he successfully translated these preclinical findings.

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